Elsewhere I explained my notion of why mitochondrial dysfunction may contribute to NASH.

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I threw that out off the top of my head as a possible example because of it's implication in inflammation. Inflammation can cause mitochondrial dysfunction and that dysfunction further exacerbates inflammation. Inflammation decreases T3 and T4 levels. T3 controls many mitochondrial activities and very low levels can cause mitochondrial dysfunction. Like all activity pathways in the body it's feedback loops within feedback loops. So the question becomes what came first the chicken (T3) or the egg (inflammation).

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That got me interested in the interplay of DIO1 (converts T4 to T3) and inflammation. I ran across something interesting with DIO3 in a white paper.

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The link between TH metabolism and oxidative stress is well established. D3 activity is increased in various models of oxidative stress. This increase in D3 activity and transcription is mediated via the ERK and p38 MAPK pathways
https://academic.oup.com/endo/article/157/8/3...ogin=false

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DIO3 converts T3 to T2 and T4 to rT3. Both T2 and rT3 are biologically inactive versions of T3 and T4. It would seem that inflammation driven upregulation of ERK and p38 expression may lead to lower levels of T3 and T4.

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Someone with very good knowledge thought that a dysregulated Hypothalamic Pituitary Axis response to inflammation may be the cause of low T3/T4 in NASH.